Archive for the ‘Triathlon’ Category

Researchers at The University of Auckland have shown for the first time that the mere presence of carbohydrate solution in the mouth immediately boosts muscle strength, even before it is swallowed.

The results suggest that a previously unknown neural pathway is activated when receptors in the mouth detect carbohydrate, stimulating parts of the brain that control muscle activity and producing an increase in muscle strength.

Previous research had shown that the presence of carbohydrate in the mouth can improve physical performance during prolonged activity, but the mechanism involved was not known and it was unclear whether a person must be fatigued for the effect to be seen.

“There appears to be a pathway in the brain that tells our muscles when energy is on the way,” says lead researcher Dr Nicholas Gant from the Department of Sport and Exercise Science.

“We have shown that carbohydrate in the mouth produces an immediate increase in neural drive to both fresh and fatigued muscle and that the size of the effect is unrelated to the amount of glucose in the blood or the extent of fatigue.”

The current research has been published in the journal Brain Research and has also captured the attention of New Scientist magazine.

In the first of two experiments, 16 healthy young men who had been doing biceps exercises for 11 minutes were given a carbohydrate solution to drink or an identically flavored energy-free placebo. Their biceps strength was measured before and immediately afterward, as was the activity of the brain pathway known to supply the biceps.

Around one second after swallowing the drink, neural activity increased by 30 percent and muscle strength two percent, with the effect lasting for around three minutes. The response was not related to the amount of glucose in the bloodstream or how fatigued the participants were.

“It might not sound like much, but a two percent increase in muscle strength is enormous, especially at the elite level. It’s the difference between winning an Olympic medal or not,” says co-author Dr Cathy Stinear.

As might be expected, a second boost in muscle strength was observed after 10 minutes when carbohydrate reached the bloodstream and muscles through digestion, but no additional boost in neural activity was seen at that time.

“Two quite distinct mechanisms are involved,” says Dr Stinear. “The first is the signal from the mouth via the brain that energy is about to be available and the second is when the carbohydrate actually reaches the muscles and provides that energy,” says Dr Stinear.

“The carbohydrate and placebo solutions used in the experiment were of identical flavor and sweetness, confirming that receptors in the mouth can process other sensory information aside from the basic taste qualities of food. The results suggest that detecting energy may be a sixth taste sense in humans,” says Dr Gant.

In the second experiment, 17 participants who had not been doing exercise and were not fatigued simply held one of the solutions in their mouths without swallowing. Measurements of the muscle between the thumb and index finger were taken while the muscle was either relaxed or active.

A similar, though smaller effect was observed as in the first experiment, with a nine percent increase in neural activity produced by the carbohydrate solution compared with placebo. This showed that the response is seen in both large powerful muscles and in smaller muscles responsible for fine hand movements.

“Together the results show that carbohydrate in the mouth activates the neural pathway whether or not muscles are fatigued. We were surprised by this, because we had expected that the response would be part of the brain’s sophisticated system for monitoring energy levels during exercise,” says Dr Stinear.

“Seeing the same effect in fresh muscle suggests that it’s more of a simple reflex – part of our basic wiring – and it appears that very ancient parts of the brain such as the brainstem are involved. Reflexive movements in response to touch, vision and hearing are well known but this is the first time that a reflex linking taste and muscle activity has been described,” she says.

Further research is required to determine the precise mechanisms involved and to learn more about the size of the effect on fresh versus fatigued muscle.

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Article adapted by MD Sports from original press release.
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Contact: Pauline Curtis
The University of Auckland

Duke University Medical Center researchers have identified the skeletal muscle changes that occur in response to endurance exercise and have better defined the role of vascular endothelial growth factor (VEGF) in creating new blood vessels, known as angiogenesis, in the process.

VEGF is a protein known to trigger blood vessel growth by activating numerous genes involved in angiogenesis.
The researchers’ new insights could provide a roadmap for medical investigators as they seek to use VEGF in treating human conditions characterized by lack of adequate blood flow, such as coronary artery disease or peripheral arterial disease.
Using mice as animal models, the researchers found that exercise initially stimulates the production of VEGF, which then leads to an increase in the number of capillaries within a specific muscle fiber type, ultimately leading to an anaerobic to aerobic change in the muscle fibers supplied by those vessels. The VEGF gene produces a protein that is known to trigger blood vessel growth.
The results of the Duke experiments were presented by cardiologist Richard Waters, M.D., Nov. 8, 2004, at the American Heart Association’s annual scientific sessions in New Orleans.
“It is known that exercise can improve the symptoms of peripheral arterial disease in humans and it has been assumed that angiogenesis played a role in this improvement,” Waters said. “However, the clinical angiogenesis trials to date utilizing VEGF have been marginally successful and largely disappointing, so we felt it would be better at this point to return to animal studies in an attempt to better understand the angiogenic process.”
The Duke team performed their experiments using a mouse model of voluntary exercise. This experimental approach is important, they explained, because most skeletal muscle adaptation studies utilize electrical stimulation of the muscle, which is much less physiologic and does not as closely mimic what would be expected in human exercise.
When placed in the dark with a running wheel, mice will instinctively run, the researchers said. In the Duke experiments, 41 out of 42 mice “ran” up to seven miles each night. At regular intervals over a 28-day period, the researchers then performed detailed analysis of capillary growth and the subsequent changes in muscle fiber type and compared these findings to sedentary mice.
Mammalian muscle is generally made up of two different fiber types – slow-twitch fibers requiring oxygen to function, and the fast-twitch fibers, which function in the absence of oxygen by breaking down glucose. Because of their need for oxygen, slow-twitch fibers tend to have a higher density of capillaries.
“Exercise training is probably the most widely utilized physiological stimulus for skeletal muscle, but the mechanisms underlying the adaptations muscle fibers make in response to exercise is not well understood,” Waters said. “What we have shown in our model is that increases in the capillary density occur before a significant change from fast-twitch to slow-twitch fiber type, and furthermore, that changes in levels of the VEGF protein occur before the increased capillary density.”
“Interestingly, capillary growth appears to occur preferentially among fast-twitch fibers, and it is these very fibers that likely change to slow-twitch fibers,” Waters said. “Since exercise has the potential to impact an enormous number of clinical conditions, therapeutic manipulations intended to alter the response to exercise would benefit from a more detailed understanding of what actually happens to muscle as a result of exercise.”
The exact relationship between VEGF, exercise induced angiogenesis, and muscle fiber type adaptation is still not clear and will become the focus of the group’s continuing research. The findings from the current study, however, are providing important temporal and spatial clues to the adaptability process.
“Our data suggests that angiogenesis is one of the key early steps in skeletal muscle adaptation and may be an essential step in the adaptability process,” Waters continued. “This understanding could be crucial for designing new studies that can be performed to inhibit the angiogenic response to exercise in order to directly test the links between angiogenesis and skeletal muscle plasticity.”
###
The research team was supported by grants from the American Heart Association and the U.S. Department of Veterans Affairs.
Other members of the Duke team were Ping Li, Brian Annex, M.D., and Zhen Yan, Ph.D. Svein Rotevatn, Haukeland University Hospital, Bergen, Norway, was also a member of the team.

Duke University Medical Center researchers have identified the skeletal muscle changes that occur in response to endurance exercise and have better defined the role of vascular endothelial growth factor (VEGF) in creating new blood vessels, known as angiogenesis, in the process.

VEGF is a protein known to trigger blood vessel growth by activating numerous genes involved in angiogenesis.

The researchers’ new insights could provide a roadmap for medical investigators as they seek to use VEGF in treating human conditions characterized by lack of adequate blood flow, such as coronary artery disease or peripheral arterial disease.

Using mice as animal models, the researchers found that exercise initially stimulates the production of VEGF, which then leads to an increase in the number of capillaries within a specific muscle fiber type, ultimately leading to an anaerobic to aerobic change in the muscle fibers supplied by those vessels. The VEGF gene produces a protein that is known to trigger blood vessel growth.

The results of the Duke experiments were presented by cardiologist Richard Waters, M.D., Nov. 8, 2004, at the American Heart Association’s annual scientific sessions in New Orleans.

“It is known that exercise can improve the symptoms of peripheral arterial disease in humans and it has been assumed that angiogenesis played a role in this improvement,” Waters said. “However, the clinical angiogenesis trials to date utilizing VEGF have been marginally successful and largely disappointing, so we felt it would be better at this point to return to animal studies in an attempt to better understand the angiogenic process.”

The Duke team performed their experiments using a mouse model of voluntary exercise. This experimental approach is important, they explained, because most skeletal muscle adaptation studies utilize electrical stimulation of the muscle, which is much less physiologic and does not as closely mimic what would be expected in human exercise.

When placed in the dark with a running wheel, mice will instinctively run, the researchers said. In the Duke experiments, 41 out of 42 mice “ran” up to seven miles each night. At regular intervals over a 28-day period, the researchers then performed detailed analysis of capillary growth and the subsequent changes in muscle fiber type and compared these findings to sedentary mice.

Mammalian muscle is generally made up of two different fiber types – slow-twitch fibers requiring oxygen to function, and the fast-twitch fibers, which function in the absence of oxygen by breaking down glucose. Because of their need for oxygen, slow-twitch fibers tend to have a higher density of capillaries.

“Exercise training is probably the most widely utilized physiological stimulus for skeletal muscle, but the mechanisms underlying the adaptations muscle fibers make in response to exercise is not well understood,” Waters said. “What we have shown in our model is that increases in the capillary density occur before a significant change from fast-twitch to slow-twitch fiber type, and furthermore, that changes in levels of the VEGF protein occur before the increased capillary density.”

“Interestingly, capillary growth appears to occur preferentially among fast-twitch fibers, and it is these very fibers that likely change to slow-twitch fibers,” Waters said. “Since exercise has the potential to impact an enormous number of clinical conditions, therapeutic manipulations intended to alter the response to exercise would benefit from a more detailed understanding of what actually happens to muscle as a result of exercise.”

The exact relationship between VEGF, exercise induced angiogenesis, and muscle fiber type adaptation is still not clear and will become the focus of the group’s continuing research. The findings from the current study, however, are providing important temporal and spatial clues to the adaptability process.

“Our data suggests that angiogenesis is one of the key early steps in skeletal muscle adaptation and may be an essential step in the adaptability process,” Waters continued. “This understanding could be crucial for designing new studies that can be performed to inhibit the angiogenic response to exercise in order to directly test the links between angiogenesis and skeletal muscle plasticity.”

 

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Article adapted by MD Sports from original press release.
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Contact: Richard Merritt
Duke University Medical Center 

The research team was supported by grants from the American Heart Association and the U.S. Department of Veterans Affairs

WESTCHESTER, Ill. – Athletes who get an extra amount of sleep are more likely to improve their performance in a game, according to a research abstract presented at the 21st Annual Meeting of the Associated Professional Sleep Societies (APSS).

The study, authored by Cheri Mah of Stanford University, was conducted on six healthy students on the Stanford men’s basketball team, who maintained their typical sleep-wake patterns for a two-week baseline followed by an extended sleep period in which they obtained as much extra sleep as possible. To assess improvements in athletic performance, the students were judged based on their sprint time and shooting percentages.

Significant improvements in athletic performance were observed, including faster sprint time and increased free-throws. Athletes also reported increased energy and improved mood during practices and games, as well as a decreased level of fatigue.

“Although much research has established the detrimental effects of sleep deprivation on cognitive function, mood and performance, relatively little research has investigated the effects of extra sleep over multiple nights on these variables, and even less on the specific relationship between extra sleep and athletic performance. This study illuminated this latter relationship and showed that obtaining extra sleep was associated with improvements in indicators of athletic performance and mood among members of the men’s basketball team.”

The amount of sleep a person gets affects his or her physical health, emotional well-being, mental abilities, productivity and performance. Recent studies associate lack of sleep with serious health problems such as an increased risk of depression, obesity, cardiovascular disease and diabetes.
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Article adapted by MD Sports from original press release.
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Contact: Jim Arcuri
American Academy of Sleep Medicine 

Experts recommend that adults get between seven and eight hours of sleep each night to maintain good health and optimum performance.

Persons who think they might be suffering from a sleep disorder are encouraged to consult with their primary care physician, who will refer them to a sleep specialist.

The annual SLEEP meeting brings together an international body of 5,000 leading researchers and clinicians in the field of sleep medicine to present and discuss new findings and medical developments related to sleep and sleep disorders.

More than 1,000 research abstracts will be presented at the SLEEP meeting, a joint venture of the American Academy of Sleep Medicine and the Sleep Research Society. The four-day scientific meeting will bring to light new findings that enhance the understanding of the processes of sleep and aid the diagnosis and treatment of sleep disorders such as insomnia, narcolepsy and sleep apnea.

Trying to reap the health benefits of exercise? Forget treadmills and spin classes, researchers at the Salk Institute for Biological Studies may have found a way around the sweat and pain. They identified two signaling pathways that are activated in response to exercise and converge to dramatically increase endurance.

The team of scientists, led by Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute’s Gene Expression Laboratory report in the July 31 advance online edition of the journal Cell that simultaneously triggering both pathways with oral drugs turned laboratory mice into long-distance runners and conferred many of exercise’s other benefits.

In addition to their allure for endurance athletes, drugs that mimic the effects of exercise have therapeutic potential in treating certain muscle diseases, such as wasting and frailty, hospital patients unable to exercise, veterans and others with disabilities as well as obesity and a slew of associated metabolic disorders where exercise is known to be beneficial.

Previous work with genetically engineered mice in the Evans lab had revealed that permanently activating a genetic switch known as PPAR delta turned mice into indefatigable marathon runners. In addition to their super-endurance, the altered mice were resistant to weight gain, even when fed a high-fat diet that caused obesity in ordinary mice. On top of their lean and mean physique, their response to insulin improved, lowering levels of circulating glucose.

“We wanted to know whether a drug specific for PPAR delta would have the same beneficial effects,” says Evans. “Genetic engineering in humans, commonly known as gene doping when mentioned in connection with athletic performance, is certainly feasible but very impractical.”

An investigational drug, identified only as GW1516 (and not commercially available), fit the bill. When postdoctoral researcher and lead author Vihang A. Narkar, Ph.D., fed the substance to laboratory mice over a period of four weeks, the researchers were in for a surprise.

“We got the expected benefits in lowering fatty acids and blood glucose levels but no effect, absolutely none, on exercise performance,” says Narkar. Undeterred, he put mice treated with GW1516 on a regular exercise regimen and every day had them run up to 50 minutes on a treadmill.

Now the exact same drug that had shown no effect in sedentary animals improved endurance by 77 percent over exercise alone and increased the portion of “non-fatiguing” or “slow twitch” muscle fibers by 38 percent. The result, while very dramatic, gave rise to a vexing question: Why is exercise so important?

First and foremost, exercise depletes muscles’ energy store, a chemical known as ATP. In times of high demand, ATP releases all its energy and forms AMP. Rising AMP levels alert AMPK, a metabolic master regulator, which acts like a gas gauge that the cell is running on empty and revs up the production of ATP. “That led us to consider whether AMPK activation was the critical trigger that allowed PPAR delta to work,” recalls Narkar.

Usually, AMPK can be found in the cytoplasm, the compartment that surrounds the nucleus, but the Salk researchers’ experiment revealed that some exercise-activated AMPK molecules slip into the nucleus. There they physically interact with PPAR delta and increase its ability to turn on the genetic network that increases endurance.

“It essentially puts a turbo charge on PPAR delta, which explains why exercise is so important,” says Evans.

Then came the ultimate couch potato experiment. The researchers fed untrained mice AICAR, a synthetic AMP analog that directly activates AMPK. After only four weeks and without any prior training, these mice got up and ran 44 percent longer than untreated, untrained mice. “That’s as much improvement as we get with regular exercise,” says Narkar.

“Exercise in a pill” might sound tempting to couch potatoes and Olympic contenders alike, but the dreams of the latter might be cut short. Evans developed a test that can readily detect GW1516 and its metabolites as well as AICAR in blood and urine and is already working with officials at the World Anti-Doping Association, who are racing to have a test in place in time for this year’s Summer Olympics.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Gina Kirchweger
Salk Institute

The study was supported by the Howard Hughes Medical Institute, the Hillblom Foundation and the National Institute of Health.

Researchers who contributed to the work include postdoctoral researchers Michael Downes, Ph.D., Ruth T. Yu, Ph.D., doctoral candidate Emi Embler, B.S., research associates Michael C. Nelson, B.S., Yuhua Zou, M.S., Ester Banayo, and Henry Juguilon, in the Gene Expression Laboratory, doctoral candidate M. Mihaylova, and assistant professor Reuben Shaw, Ph.D., in the Molecular and Cell Biology Laboratory, assistant professor Yong-Xu Wang, Ph.D., at the University of Massachusetts Medical School, Massachusetts, and professor Heonjoon Kang, Ph.D., at the School of Earth and Environmental Sciences, Seoul National University, South Korea.

Energy bars, touted for improving athletic performance while providing the right combination of essential nutrients, may not always give endurance athletes the boost they expect.An Ohio State University researcher compared two popular energy bars and found that one of the bars didn’t give the moderate increase in blood sugar known to enhance performance in endurance athletes. Instead, its effect was much like a candy bar – giving a big rush of sugar to the blood, followed by a sharp decline.

“Theoretically, energy bars produce more moderate increases and decreases in blood sugar levels than a typical candy bar,” said Steve Hertzler, an associate professor of medical dietetics at Ohio State. “But these claims aren’t necessarily valid.” His study appears in a recent issue of the Journal of the American Dietetic Association.

Hertzler wanted to know how energy bars affected blood glucose levels. Glucose is a sugar that provides energy to the body’s cells – for example, red-blood cells and most parts of the brain derive most of their energy from glucose.

“Athletes – especially those involved in endurance sports – want to enhance performance, and energy bars claim to help keep blood sugar levels at a moderate level,” Hertzler said.

Volunteers had to fast for at least 12 hours before taking part in each of four experiments. Then, they ate one of four experimental “meals” consisting of either four slices of white bread; a Snickers bar; an Ironman PR Bar; or a PowerBar. Each experimental meal provided the same amount of carbohydrates (50 grams.)

Hertzler then tested the effects these foods had on blood glucose levels at 15-minute intervals for up to two hours after each experimental meal. The volunteers had to wait at least 24 hours between each experimental meal.

Hertzler measured each subject’s blood samples for glucose levels, to determine which food most raised blood sugar levels.

Both energy bars caused blood glucose levels to peak at 30 minutes, while levels peaked at 45 minutes after the bread and candy bar were consumed. Blood glucose levels declined steadily throughout the duration of testing for all foods but the Ironman PR Bar. This bar caused blood glucose rates to remain fairly steady, probably because of the moderate carbohydrate level of the bar, according to Hertzler.

“Though blood glucose rates peaked at 30 minutes with both bars, the high-carbohydrate energy bar – the PowerBar – caused a much sharper decline,” Hertzler said. “In fact, the decline was sharper than with the candy bar.” Much of the energy derived from the bread and the candy bar came from carbohydrate and the same was true for the PowerBar. While the bar is low in protein and fat, more than 70 percent of it is made up of carbohydrate (such as high-fructose corn syrup; oat bran; and brown rice). In contrast, 40 percent of the Ironman PR is comprised of carbohydrate (high fructose corn syrup and fructose.) The rest of the bar was comprised of 30 percent fat and 30 percent protein.

“The composition of this bar may have been responsible for the diminished blood glucose response,” Hertzler said. “Athletes involved in short-duration events who want a quick energy boost should eat a high-carbohydrate energy bar or a candy bar,” he suggests. “However, endurance athletes would do well to consume an energy bar with a moderate carbohydrate level.”

Hertzler conducted this study while at Kent State University in Kent, Ohio. He is continuing similar research at Ohio State.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Steve Hertzler
Ohio State University

Editor’s note: This research was funded by a grant from Kent State University. The researcher received no funding from either energy bar manufacturer.

Female athletes often lose their menstrual cycle when training strenuously, but researchers have long speculated on whether this infertility was due to low body fat, low weight or exercise itself. Now, researchers have shown that the cause of athletic amenorrhea is more likely a negative energy balance caused by increasing exercise without increasing food intake.”A growing proportion of women are susceptible to losing their menstrual cycle when exercising strenuously,” says Dr. Nancy I. Williams, assistant professor of kineseology and physiology at Penn State. “If women go six to 12 months without having a menstrual cycle, they could show bone loss. Bone densities in some long distance runners who have gone for a prolonged time period without having normal menstrual cycles can be very low.”

In studies done with monkeys, which show menstrual cyclicity much like women, researchers showed that low energy availability associated with strenuous exercise training plays an important role in causing exercise-induced amenorrhea. These researchers, working at the University of Pittsburgh, published findings in the Journal of Clinical Endocrinology and Metabolism showing that exercise-induced amenorrhea was reversible in the monkeys by increasing food intake while the monkeys still exercised.

Williams worked with Judy L. Cameron, associate professor of psychiatry and cell biology and physiology at the University of Pittsburgh. Dana L. Helmreich and David B. Parfitt, then graduate students, and Anne Caston-Balderrama, at that time a post-doctoral fellow at the University of Pittsburgh, were also part of the research team. The researchers decided to look at an animal model to understand the causes of exercise-induced amenorrhea because it is difficult to closely control factors, such as eating habits and exercise, when studying humans. They chose cynomolgus monkeys because, like humans, they have a menstrual cycle of 28 days, ovulate in mid-cycle and show monthly periods of menses.

“It is difficult to obtain rigorous control in human studies, short of locking people up,” says Williams.

Previous cross-sectional studies and short-term studies in humans had shown a correlation between changes in energy availability and changes in the menstrual cycle, but those studies were not definitive.

There was also some indication that metabolic states experienced by strenuously exercising women were similar to those in chronically calorie restricted people. However, whether the increased energy utilization which occurs with exercise or some other effect of exercise caused exercise-induced reproductive dysfunction was unknown.

“The idea that exercise or something about exercise is harmful to females was not definitively ruled out,” says Williams. “That exercise itself is harmful would be a dangerous message to put out there. We needed to look at what it was about exercise that caused amenorrhea, what it was that suppresses ovulation. To do that, we needed a carefully controlled study.”

After the researchers monitored normal menstrual cycles in eight monkeys for a few months, they trained the monkeys to run on treadmills, slowly increasing their daily training schedule to about six miles per day. Throughout the training period the amount of food provided remained the standard amount for a normal 4.5 to 7.5 pound monkey, although the researchers note that some monkeys did not finish all of their food all of the time.

The researchers found that during the study “there were no significant changes in body weight or caloric intake over the course of training and the development of amenorrhea.” While body weight did not change, there were indications of an adaptation in energy expenditure. That is, the monkeys’ metabolic hormones also changed, with a 20 percent drop in circulating thyroid hormone, suggesting that the suppression of ovulation is more closely related to negative energy balance than to a decrease in body weight.

To seal the conclusion that a negative energy balance was the key to exercise-induced amenorrhea, the researchers took four of the previous eight monkeys and, while keeping them on the same exercise program, provided them with more food than they were used to. All the monkeys eventually resumed normal menstrual cycles. However, those monkeys who increased their food consumption most rapidly and consumed the most additional food, resumed ovulation within as little as 12 to 16 days while those who increased their caloric intake more slowly, took almost two months to resume ovulation.

Williams is now conducting studies on women who agree to exercise and eat according to a prescribed regimen for four to six months. She is concerned because recreational exercisers have the first signs of ovulatory suppression and may easily be thrust into amenorrhea if energy availability declines. Many women that exercise also restrict their calories, consciously or unconsciously.

“Our goal is to test whether practical guidelines can be developed regarding the optimal balance between calories of food taken in and calories expended through exercise in order to maintain ovulation and regular menstrual cycles,” says Williams. “This would then ensure that estrogen levels were also maintained at healthy levels. This is important because estrogen is a key hormone in the body for many physiological systems, influencing bone strength and cardiovascular health, not just reproduction.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: A’ndrea Elyse Messer
Penn State

The old adage “use it or lose it” is truer than ever. People who maintain a vigorously active lifestyle as they age gain less weight than people who exercise at more moderate levels, according to a first-of-its-kind study that tracked a large group of runners who kept the same exercise regimen as they grew older. The study also found that maintaining exercise with age is particularly effective in preventing extreme weight gain, which is associated with high blood pressure, high cholesterol, diabetes, and other diseases.

The study, conducted by Paul Williams of the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab), followed 6,119 men and 2,221 women who maintained their weekly running mileage (to within three miles per week) over a seven-year period. On average, the men and women who ran over 30 miles per week gained half the weight of those who ran less than 15 miles per week.

“To my knowledge, this is the only study of its type,” says Williams, a staff scientist in Berkeley Lab’s Life Sciences Division. “Other studies have tracked exercise over time, but the majority of people will have changed their exercise habits considerably.”

The research is the latest report from the National Runners’ Health Study, a 20-year research initiative started by Williams that includes more than 120,000 runners. It appears in the May issue of the journal Medicine and Science in Sports and Exercise.

Specifically, between the time subjects entered the study and when they were re-contacted seven years later, 25-to-34-year-old men gained 1.4 pounds annually if they ran less than 15 miles per week. In addition, male runners gained 0.8 pounds annually if they ran between 15 and 30 miles per week, and 0.6 pounds annually if they ran more than 30 miles per week.

This trend is mirrored in women. Women between the ages of 18 and 25 gained about two pounds annually if they ran less than 15 miles per week, 1.4 pounds annually if they ran 15 to 30 miles per week, and slightly more than three-quarters of a pound annually if they ran more than 30 miles per week. Other benefits to running more miles each week included fewer inches gained around the waist in both men and women, and fewer added inches to the hips in women.

“As these runners aged, the benefits of exercise were not in the changes they saw in their bodies, but how they didn’t change like the people around them,” says Williams.

Although growing older and gaining weight is something of a package deal, it isn’t the same in everyone. The lucky few remain lean as they age, most people pack on several pounds, and some people become obese. The latter group is particularly at risk for high blood pressure, high cholesterol, and diabetes. Fortunately, Williams’ results show that maintaining exercise can combat such extreme weight gain.

“Getting people to commit to a vigorously active lifestyle while young and lean will go a long way to reducing the obesity epidemic in this country,” says Williams.

Another paper published in the November 2006 issue of the journal Obesity by Williams and Paul Thompson of Hartford (CT) Hospital found that runners who increased their running mileage gained less weight than those who remained sedentary, and runners that quit running became fatter.

“The time to think about exercise is before you think you need it,” says Williams. “The medical journals are full of reports on how difficult it is to regain the slenderness of youth. The trick is not to get fat.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: Dan Krotz
DOE/Lawrence Berkeley National Laboratory

Williams’ research was funded by the National Heart, Lung and Blood Institute. The study in the May issue of the journal Medicine and Science in Sports and Exercise is entitled Maintaining Vigorous Activity Attenuates 7-yr Weight Gain in 8,340 Runners.